The protein p53 as a transcription factor with strong tumor-suppressive activities is known to trigger apoptosis via multiple pathways and is directly involved in the recognition of DNA damage and DNA repair processes. P53 alteration is now recognized as a common event in the pathogenesis of many types of human malignancies. Deregulation of tumor suppressor p53 pathways plays an important role in the activation of cell proliferation or inactivation of apoptotic cell death during carcinogenesis and tumor progression. Mounting evidence indicates that the p53 status of tumors and also the regulatory functions of p53 may be relevant to the long noncoding RNAs (lncRNA)-dependent gene regulation programs. Besides coding genes, lncRNAs that do not encode for proteins are induced or suppressed by p53 transcriptional response and thus control cancer progression. https://www.selleckchem.com/products/LBH-589.html LncRNAs also have emerged as key regulators that impinge on the p53 signaling network orchestrating global gene-expression profile. Studies have suggested that aberrant expression of lncRNAs as a molecular-genomic signature may play important roles in cancer biology. Accordingly, it is important to elucidate the mechanisms by which the crosstalk between lncRNAs and p53 occurs in the development of numerous cancers. Here, we review how several classes of lncRNAs and p53 pathways are linked together in controlling the cell cycle and apoptosis in various cancer cells in both human and mouse model systems.Long noncoding RNAs (lncRNAs) are widely known for their regulatory function in transcriptional and posttranscriptional processes. The involvement of such non-protein-coding RNAs in nuclear organization and chromatin remodeling is often associated with an increased risk of human malignancies. In cancer, lncRNAs either promote cell survival or may act as a growth suppressor, thus conferring a key regulatory function other than their established role in fundamental cellular processes. Interestingly, lncRNAs interfere with the stages of apoptosis and related pathways involving p53. Many of these molecules either regulate or are regulated by p53 while mounting oncogenic events. Consequently, they may confer both prosurvival or proapoptotic functions depending upon the tissue type. Since the mechanism of cell death is bypassed in many human cancers, it has emerged that the lncRNAs are either overexpressed or knocked down to sensitize cells to apoptotic stimuli. Nonetheless, the abundant expression of lncRNAs in tumor cells renders them suitable targets for anticancer therapies. Although the role of lncRNAs in the p53 network and apoptosis has been independently defined, their interplay in activating p53-target genes during cell cycle arrest remains unexplored. Thus, we have specifically reviewed the possible involvement of lncRNAs in the p53-mediated apoptosis of human cancer cells. In particular, we summarize the growing evidence from individual studies and analyze whether lncRNAs are essential to facilitate apoptosis in a p53-dependent manner. This may lead to the identification of p53-associated lncRNAs that are suitable therapeutic targets or diagnostic/prognostic markers.TET1 mediates demethylation in tumors, but its role in diabetic nephropathy (DN), a prevalent diabetic complication, is unclear. We attempted to probe the possible mechanism of TET1 in DN. A DN rat model was established and verified by marker detection and histopathological observation. The in vitro model was established on human mesangial cells (HMCs) induced by high glucose (HG), and verified by evaluation of fibrosis and inflammation. The differentially expressed mRNA was screened out by microarray analysis. The most differentially expressed mRNA (TET1) was reduced in DN rats and HG-HMCs. The upstream and downstream factors of TET1 were verified, and their roles in DN were analyzed by gain- and loss-function assays. TET1 was decreased in DN rats and HG-HMCs. High expression of TET1 decreased biochemical indexes and renal injury of DN rats and hampered the activity, fibrosis, and inflammation of HG-HMCs. Ap1 lowered TET1 expression, and enhanced inflammation in HG-HMCs, and accentuated renal injury in DN rats. TET1 overexpression inhibited the effect of Ap1 on DN. TET1 promoted the transcription of Nrf2. The Ap1/TET1 axis mediated the Nrf2/ARE pathway activity. Overall, TET1 overexpression weakened the inhibitory effect of Ap1 on the Nrf2/ARE pathway, thus alleviating inflammation and renal injury in DN.Marine picoplankton contribute to global carbon sequestration and nutrient recycling. These processes are directly related to the composition of communities, which in turn depends on microbial interactions and environmental forcing. Under regular seasonal cycles, marine communities show strong predictable patterns of annual re-occurrences, but little is known about the effect of environmental perturbation on their organization. The aim of our study was to investigate the co-occurrence patterns of planktonic picoeukaryote, bacteria and archaea under contrasting environmental conditions. The study was designed to have high sampling frequency that could match both the biological rhythm of marine microbes and the short time scale of extreme weather events. Our results show that microbial networks changed from year to year depending on conditions. In addition, individual taxa became less interconnected and changed neighbours, which revealed an unfaithful relationship between marine microorganisms. This unexpected pattern suggests possible switches between organisms that have similar specific functions, or hints at the presence of organisms that share similar environmental niches without interacting. Despite the observed annual changes, the time series showed re-occurring communities that appear to recover from perturbations. Changing co-occurrence patterns between marine microorganisms may allow the long-term stability of ecosystems exposed to contrasting meteorological events.The in situ formation of reduced dimensional perovskite layer via post-synthesis ion exchange has been an effective way of passivating organic-inorganic hybrid perovskites. In contrast, cesium ions in Cs-based inorganic perovskite with strong ionic binding energy cannot exchange with those well-known organic cations to form reduced dimensional perovskite. Herein, we demonstrate that tetrabutylammonium (TBA+ ) cation can intercalate into CsPbI3 to effectively substitute the Cs cation and to form one-dimensional (1D) TBAPbI3 layer in the post-synthesis TBAI treatment. Such TBA cation intercalation leads to in situ formation of TBAPbI3 protective layer to heal defects at the surface of inorganic CsPbI3 perovskite. The TBAPbI3 -CsPbI3 perovskite exhibited enhanced stability and lower defect density, and the corresponding perovskite solar cell devices achieved an improved efficiency up to 18.32?% compared to 15.85?% of the control one.